When synapses are stimulated repetitively, the strength of transmission increases or decreases, processes called facilitation and depression, respectively. While depression can potentially influence information processing, the mechanisms of its onset or its regulation have not been worked out yet at synapses of the central nervous system. Mechanisms of short-term synaptic depression will be examined at the endbulb synapses in the avian nucleus magnocellularis (nMAG). The proposed experimental work has the following aims: (1) Determine whether short-term synaptic depression can be interpreted as a decrease in the number of available releasable synaptic vesicles or as a decrease in their release probability. This experimental series will also serve to examine what is the relationship between extracellular calcium concentration and transmitter release at depressed synapses. (2) Test the hypothesis that synaptic depression at the endbulb synapse is due to the action of a glutamate autoreceptor. In experimental series (1) and (2) excitatory postsynaptic currents will be elicited by electrical shocks delivered to fibres of the auditory nerve and recorded from neurons of nMAG in brain slices using the patch clamp technique. (3) Determine the role of presynaptic calcium current inactivation in the onset of synaptic depression. Presynaptic terminals of auditory nerve fibres will be voltage clamped and calcium current isolated. Calcium current will be activated by applying voltage commands that approximate the action potential waveform.